Inhalation injury to tracheal epithelium in an ovine model of cotton smoke exposure. Early phase (30 minutes).
ABSTRACT The purpose of this study was to evaluate lung cell injury during the acute phase of smoke inhalation injury. A group of 10 sheep were anesthetized with halothane and pancuronium followed by endotracheal intubation. In the first experiment 5 sheep were given air (sham group) and 5 were insufflated with cooled cotton smoke with a modified bee smoker. In the second part of our study (Experiment 2) the animals were insufflated with the following number of smoke breaths: 1 x 12 (n = 3); 2 x 12 (n = 4); 3 x 12 (n = 4) 4 x 12 (n = 4); and sham control (n = 1). After 30 min the animals were killed with KCl and the trachea prepared for scanning, transmission electron, and light microscopy. Our initial observation with scanning electron microscopy revealed a large amount of mucus on the surface of the epithelia. Numerous ciliated cells had been sloughed from the epithelium and were observed on the surface of the remaining ciliated cells. The sloughed cells were intact, and the cilia remained on the apical cell surface. Light and transmission electron microscopy revealed that most goblet cells were in the process of extruding mucus. The cytoplasm of goblet and basal cells appeared normal. Ciliated cells had a slightly vesiculated cytoplasm, and many were in the process of being sloughed from the epithelial surface. In these cells desmosomal attachment had been separated. The light microscope evaluation of the tracheal epithelium showed there was no dose-dependent effect between the four treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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ABSTRACT: The bronchial epithelium is the major barrier between the host and the provoking antigens in bronchial asthma. Recent studies have indicated that the epithelium is a truly stratified structure, with the superficial columnar cells depending on the underlying basal cells for anchorage. Only columnar cells are shed into bronchial lavage fluid. The epithelium is more fragile in asthma and more cells are lost in clusters. Desmosomes appear to be the major structural adhesion mechanism at the plane of cleavage between the columnar cells and the basal cells. The alpha 6- and beta 4-integrins, which contribute to hemidesmosomes and anchor cells to the underlying basement membrane, are expressed solely by basal cells. The apical aspects of the columnar cells are sealed by tight and intermediate junctions. There is constitutive expression of ICAM-1 and E-selectin in the vasculature of the bronchial mucosa, and ICAM is also present within the epithelium. These findings indicate that the bronchial epithelium is a complex structure that, as a mucosal surface, has constitutive expression of inflammatory cell adhesion molecules to serve normal leukocyte traffic.The American review of respiratory disease 01/1994; 148(6 Pt 2):S79-82. · 10.19 Impact Factor
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ABSTRACT: Smoke inhalation occurs in 10% to 30% of patients admitted to burn centers, and increases mortality by a maximum of 20% over that predicted by age and extent of cutaneous burn alone. Pneumonia in these patients then further increases mortality by a maximum of 40%. While one estimate suggested that 75% of deaths following burn injury may be accounted for by inhalation injury, more recent cohort studies have suggested there is a decreasing mortality attributable to inhalation injury. As part of understanding and improving outcomes from burn injuries, the pathophysiology and inflammatory processes involved in smoke inhalation injury has been extensively investigated in animal models. This review will emphasize the inflammatory pathways involved in inhalation injury, and targeted methods used to treat this injury in both experimental and human models.Inflammation & allergy drug targets. 04/2009; 8(1):63-9.